Focal brain ischemia in mice does not cause electrophysiological signs of critical illness neuropathy
Description
Background and aims: Critical illness polyneuropathy (CIP) is a common complication of severe systemic illness treated in intensive care medicine. Ischemic stroke leads to an acute critical injury of the brain with hemiparesis and immobilization and often requires extended medical treatment. In addition, stroke-induced sarcopenia contributes greatly to poor rehabilitation and immobilization and is characterized by denervation, atrophy and remodeling in the paralytic, but also to some extent the unaffected limb. In this pilot study, we asked whether signs of an underlying CIP-like phenotype occur after middle cerebral artery occlusion (MCAo) in mice. Methods: Focal brain ischemia was induced in adult male C57Bl/6 mice by a 60-minute MCAo followed by reperfusion. Nerve conduction function was measured in the ipsilateral sciatic nerve and muscle potentials were recorded in the ipsilateral gastrocnemius and quadriceps muscle with standard electroneurography/-myography on days 10, 22 and 44 after stroke. An additional crush-injury to the sciatic nerve was included in two sham-operated mice as internal positive control. Results: MCAo/ reperfusion induced functional deficits with a maximum Bederson score of 2 on day 3 and marked hemispheric brain atrophy of -27 % in histological analysis. No significant difference in large-fiber conduction function was found between MCAo and sham-operated animals, nor was there an increase in spontaneous electromyographic activity in muscles of animals in the MCAo group. In contrast, sham-operated mice with an additional crush injury of the sciatic nerve (sham+) developed marked abnormalities: reduction of the compound motor action potential amplitudes (CMAP) and motor conduction velocities (MCV) in combination with pathologic spontaneous activity (PSA), all of which had largely recovered by day 44. Conclusion: Mice showed no signs of systemic peripheral nerve dysfunction or axonal degeneration typical for a CIP-like phenotype after 60 min MCAo/ reperfusion.